curcumin and Enteritis

Three commercial broiler breeds were fed from hatch with a diet supplemented with Capsicum and Curcuma longa oleoresins, and co-infected with Eimeria maxima and Clostridium perfringens to induce necrotic enteritis (NE). Pyrotag deep sequencing of bacterial 16S rRNA showed that gut microbiota compositions were quite distinct depending on the broiler breed type. In the absence of oleoresin diet, the number of operational taxonomic units (OTUs), was decreased in infected Cobb, and increased in Ross and Hubbard, compared with the uninfected. In the absence of oleoresin diet, all chicken breeds had a decreased Candidatus Arthromitus, while the proportion of Lactobacillus was increased in Cobb, but decreased in Hubbard and Ross. Oleoresin supplementation of infected chickens increased OTUs in Cobb and Ross, but decreased OTUs in Hubbard, compared with unsupplemented/infected controls. Oleoresin supplementation of infected Cobb and Hubbard was associated with an increased percentage of gut Lactobacillus and decreased Selenihalanaerobacter, while Ross had a decreased fraction of Lactobacillus and increased Selenihalanaerobacter, Clostridium, Calothrix, and Geitlerinema. These results suggest that dietary Capsicum/Curcuma oleoresins reduced the negative consequences of NE on body weight and intestinal lesion, in part, through alteration of the gut microbiome in 3 commercial broiler breeds.

Topics: Animals; Capsicum; Chickens; Clostridium Infections; Clostridium perfringens; Coccidiosis; Curcuma; Diet; Dietary Supplements; Eimeria; Enteritis; Gastrointestinal Microbiome; Intestines; Male; Plant Extracts; Poultry Diseases; RNA, Ribosomal, 16S

The Clostridium-related poultry disease, necrotic enteritis (NE), causes substantial economic losses on a global scale. In the present study, a mixture of two plant-derived phytonutrients, Capsicum oleoresin and turmeric oleoresin (XT), was evaluated for its effects on local and systemic immune responses using a co-infection model of experimental NE in commercial broilers. Chickens were fed from hatch with a diet supplemented with XT, or with a non-supplemented control diet, and either uninfected or orally challenged with virulent Eimeria maxima oocysts at 14 d and Clostridium perfringens at 18 d of age. Parameters of protective immunity were as follows: (1) body weight; (2) gut lesions; (3) serum levels of C. perfringens α-toxin and NE B-like (NetB) toxin; (4) serum levels of antibodies to α-toxin and NetB toxin; (5) levels of gene transcripts encoding pro-inflammatory cytokines and chemokines in the intestine and spleen. Infected chickens fed the XT-supplemented diet had increased body weight and reduced gut lesion scores compared with infected birds given the non-supplemented diet. The XT-fed group also displayed decreased serum α-toxin levels and reduced intestinal IL-8, lipopolysaccharide-induced TNF-α factor (LITAF), IL-17A and IL-17F mRNA levels, while cytokine/chemokine levels in splenocytes increased in the XT-fed group, compared with the animals fed the control diet. In conclusion, the present study documents the molecular and cellular immune changes following dietary supplementation with extracts of Capsicum and turmeric that may be relevant to protective immunity against avian NE.

Topics: Animal Feed; Animals; Antibodies, Bacterial; Bacterial Toxins; Calcium-Binding Proteins; Capsicum; Clostridium Infections; Clostridium perfringens; Coccidiosis; Coinfection; Curcuma; Cytokines; Diet; Dietary Supplements; Eimeria; Enteritis; Necrosis; Plant Extracts; Poultry Diseases; Type C Phospholipases

Wheat is a major diet from many years; apart from its nutritious value, the wheat protein gliadin is responsible for many inflammatory diseases like celiac disease (CD), and non-celiac gluten sensitivity (NCGS). In this study, the gliadin-induced inflammation and associated cellular damage along with the protective role of curcumin was evaluated using human intestinal cell lines (HCT-116 and HT-29) as a model. Cells were cultured and exposed to 160 μg/ml of gliadin, 100 μM H

Topics: Anti-Inflammatory Agents; Celiac Disease; Curcumin; Cytokines; Enteritis; Gliadin; HCT116 Cells; HT29 Cells; Humans; Inflammation Mediators; Integrin alpha Chains; Integrin beta Chains; Intestinal Mucosa; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Oxidative Stress; Signal Transduction; Wheat Hypersensitivity

Intestinal mucosa barrier (IMB) dysfunction results in many notorious diseases for which there are currently few effective treatments. We studied curcumin's protective effect on IMB and examined its mechanism by using methotrexate (MTX) induced rat enteritis model and lipopolysaccharide (LPS) treated cell death model.. Curcumin was intragastrically administrated from the first day, models were made for 7 days. Cells were treated with curcumin for 30 min before exposure to LPS. Rat intestinal mucosa was collected for evaluation of pathological changes. We detected the activities of D-lactate and diamine oxidase (DAO) according to previous research and measured the levels of myeloperoxidase (MPO) and superoxide dismutase (SOD) by colorimetric method. Intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) were determined by RT-PCR and IL-10 production was determined by ELISA. We found Curcumin decreased the levels of D-lactate, DAO, MPO, ICAM-1, IL-1β and TNF-α, but increased the levels of IL-10 and SOD in rat models. We further confirmed mitogen-activated protein kinase phosphatase-1 (MKP-1) was activated but phospho-p38 was inhibited by curcumin by western blot assay. Finally, NF-κB translocation was monitored by immunofluorescent staining. We showed that curcumin repressed I-κB and interfered with the translocation of NF-κB into nucleus.. The effect of curcumin is mediated by the MKP-1-dependent inactivation of p38 and inhibition of NF-κB-mediated transcription. Curcumin, with anti-inflammatory and anti-oxidant activities may be used as an effective reagent for protecting intestinal mucosa barrier and other related intestinal diseases.

Topics: Animals; Cell Line; Curcumin; Disease Models, Animal; Dual Specificity Phosphatase 1; Enteritis; Enzyme Activation; Gene Expression Regulation; Humans; Intercellular Adhesion Molecule-1; Intestinal Mucosa; Mice; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Random Allocation; Rats; Rats, Sprague-Dawley

To observe the changes in intestinal mucosal permeability in rats with methotrexate (MTX)-induced small intestinal damage and investigate the protective effects of curcumin.. The experiment was carried out using 4 groups of rats, namely the normal control group, enteritis model group, sulfasalazine (SASP) group and curcumin group. With the exception of the rats in the normal control group, all rats were subjected to intraperitoneal MTX injection to induce enteritis and received subsequent daily intragastric administration of SASP (100 mg/kg), curcumin (100 mg/kg), or normal saline for 5 days. The disease activity index (DAI), colonic mucosal damage index (CMDI) and histological score (HS) of the rats were evaluated. The levels of diamine oxidase (DAO) and D-lactate were assessed using spectrophotometric assay, and myeloperoxidase (MPO) activity and intracellular adhesion molecule-1 (ICAM-1) protein expression were measured by biochemical and immunohistochemical methods, respectively.. Compared with the normal control group, the rats in the model group showed significantly increased DAI, CMDI and HS and levels of DAO, D-lactate, ICAM-1 and MPO. Curcumin treatment resulted in significantly decreased DAI, CMDI, HS and lowered activities of D-lactate, ICAM-1 and MPO in comparison with the model group (P<0.01).. MTX induces increased mucosal permeability of the small intestines in rats, and curcumin may offer protective effects against MTX-induced rat enteritis by lowering the intestinal mucosal permeability.

Topics: Amine Oxidase (Copper-Containing); Animals; Anti-Inflammatory Agents, Non-Steroidal; Curcumin; Enteritis; Female; Immunohistochemistry; Intercellular Adhesion Molecule-1; Intestinal Mucosa; Intestine, Small; Methotrexate; Peroxidase; Rats; Rats, Sprague-Dawley; Spectrophotometry